Search results for alpha-1

alpha 1 Antitrypsin antibody [703], Genetex, GTX40830

GDNF Receptor alpha 1 antibody, Genetex, GTX41588

Anti-Centaurin alpha 1 antibody, Abcam, AB27476

Interferon Alpha-1 (IFNA1) Antibody (Biotin), Abbexa, abx271379

Interferon Alpha-1 (IFNA1) Antibody (Biotin) is a Rabbit Polyclonal antibody conjugated to Biotin against Interferon Alpha-1 (IFNA1).

Biotin Anti-alpha 1 Antitrypsin antibody, Abcam, AB48325

Interferon Alpha-1 (IFNA1) Antibody Pair, Abbexa, abx370641

Interferon Alpha-1 (IFNA1) Antibody Pair for use in Sandwich ELISA assay development. This antibody pair contains: Component 5 × 96 tests 10 × 96 tests Capture Antibody200 µg 400 µg Biotin-Conjugated Detection Antibody 50 µg 100 µg Standard 2 µg 10 µg Please note that quantities and concentrations may change between different batches. It is recommended to use this antibody pair with abx098958 Antibody Pair Support Kit (Sandwich Method).

AMPK alpha 1 (phospho Ser496) antibody, Genetex, GTX50224

alpha 1 Catenin (phospho Ser641) antibody, Genetex, GTX50338

Sodium/Potassium ATPase alpha 1 antibody, Genetex, GTX52350

Alpha-1-antitrypsin, Human, ELISA kit, Hycult Biotech, HK387

The human alpha-1 antitripsin ELISA detects both the healthy monomeric form (M variant) and the disease associated polymeric forms (Z variants) of human alpha-1-antitrypsin with equal affinity. Alpha-1-antitrypsin is a member of the serine protease inhibitor (serpin) superfamily which are proteins known for their ability to inhibit proteases. It is the most abundant circulating protease inhibitor known. It mainly targets enzymes released by neutrophils, especially neutrophil elastase (NE) but also proteinase 3 (PR3) and Cathepsin G (CG). Serpinopathies are conformational diseases characterized by the polymerization and intracellular retention of members of the serpin superfamily. The best known is Alpha-1-antitrypsin deficiency, with the most common severe deficiency allele being the Z mutation (Glu342Lys). This severe autosomal dominant disorder causes the protein to undergo a conformational transition and form ordered polymers that are retained within hepatocytes. Due to this accumulation of polymers in hepatocytes, blood alpha-1 trypsin levels will decrease leading to chronic uninhibited tissue breakdown. This causes the degradation especially of lung tissue which will eventually lead to pulmonary emphysema. In addition, accumulation of polymers in hepatocytes causes liver diseases such as neonatal hepatitis, cirrhosis, and hepatocellular carcinoma.